This proposal deals with the neurochemical mediation of glucoprivic feeding behavior. The glucoprivic control of feeding is a control which is exercised when the brain is deprived of glucose, its primary energy substrate. Several lines of evidence suggest that noradrenergic neuron in the brain may mediate glucoprivic feeding behavior. Recently, we have attempted to test this hypothesis using a delayed feeding paradigm. This paradigm makes use of the recent discovery that glucoprivic challenges elicit a significant increase in food intake even when access to food is denied until all other signs of glucoprivation have abated. Using this delayed feeding paradigm, we can now temporally dissociate the neurochemical events associated with the ingestive response from other confounding consequences of insulin or glucoprivation. Our preliminary studies suggest that the activation of hypothalamic noradrenergic neurons during glucoprivation is uniquely and perhaps causally related to feedng behavior. Glucoprivation appears to activate these neurons and feeding behavior normalizes their activity. The goal of the proposed research is to further define the relationship between glucoprivic feeding behavior, postglucoprivic feeding behavior and the glucoprivation associated increase in hypothalamic noradrenergic neuron activity. The experiments are intended to identify the critical metabolic stimuli responsible for activating noradrenergic neurons at the onset of glucoprivation and the specific events associated with food intake which are responsible for normalizing NE neuronal activity once glucoprivation has occurred.